Research Papers:
Effects of targeting SLC1A5 on inhibiting gastric cancer growth and tumor development in vitro and in vivo
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Abstract
Jian Lu1,2,3,*, Min Chen1,3,*, Zhenhua Tao2, Sumeng Gao3, Yang Li1, Yu Cao1, Chun Lu4 and Xiaoping Zou1,3
1Department of Gastroenterology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing 210008, P.R. China
2Department of Gastroenterology, Nanjing Medical University Affiliated Wuxi Second Hospital, Wuxi 214002, P.R. China
3Department of Gastroenterology, The Affiliated Drum Tower Hospital of Nanjing University, Medical School, Nanjing 210008, P.R. China
4Department of Microbiology, Nanjing Medical University, Nanjing 211116, P.R. China
*These authors have contributed equally to this work
Correspondence to:
Chun Lu, email: [email protected]
Xiaoping Zou, email: [email protected]
Keywords: SLC1A5, gastric cancer, cell proliferation, cell motility
Received: April 15, 2017 Accepted: June 10, 2017 Published: July 22, 2017
ABSTRACT
Aims: To investigate the oncogenic effects of SLC1A5 on gastric cancer development in vitro and in vivo.
Methods: The expression level of SLC1A5 was detected in 70 gastric cancer paraffin-embedded tissues by immunohistochemistry and also was detected in gastric cancer cell lines by qRT-PCR and western blotting analysis. The effects of knockdown SLC1A5 were analyzed on cell proliferation, cell cycle, the ability of cell migration and invasion and growth signaling pathway in vitro. By using subcutaneous xenograft mouse, the importance of SLC1A5 expression was assessed for both successful engraftment and growth of gastric cancer cells in vivo.
Results: SLC1A5 was up-regulated in gastric cancer tissues and was correlated with malignant features such as deeper local invasion, higher lymph node metastasis, advanced TNM stages and higher Ki-67 expression. Knockdown SLC1A5 in gastric cancer cells suppressed cell proliferation, caused G0/G1 arrest and inhibited cell invasion as well as migration partly by inactivated mTOR/p-70S6K1 signaling pathway in vitro. Furthermore, in vivo experiments indicated that suppression of SLC1A5 could inhibit relative volume of xenografted tumor.
Conclusions: Our results suggested that SLC1A5 might be considered as a new biomarker and also as a potential therapeutic target in gastric cancer.
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